title: Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats.
abstract: The purpose of this study was to evaluate the effect of calcium antagonists on basal tension and the elevated 42K efflux in aorta from aldosterone-salt hypertensive rats. Diltiazem decreased the basal tension (2.0 +/- 0.4 g) as well as the phasic contractile activity and returned the elevated 42K efflux (0.018 +/- 0.002/min) toward control values (0.010 +/- 0.001/min, p less than 0.001). The diltiazem median inhibitory concentration (IC50) for basal tension (0.04 +/- 0.02 microM), however, was sevenfold less than the IC50 for basal 42K efflux (0.22 +/- 0.08 microM, p less than 0.01). The basal 45Ca influx in aorta from aldosterone-salt hypertensive rats (120 +/- 4 microM/l cell H2O/min) was also decreased by diltiazem in a concentration-dependent manner, whereas the 45Ca influx in aorta from control-salt rats (135 +/- 3 microM/l cell H2O/min) was not altered. Similarly, the dihydropyridine nisoldipine eliminated the basal tension (2.7 +/- 0.5 g) and returned the elevated basal 42K efflux from the hypertensive aorta toward control levels (0.010 +/- 0.0003/min, p less than 0.001). The nisoldipine IC50 for basal tension (0.016 +/- 0.01 nM) was 160-fold less than the IC50 for basal 42K efflux (1.8 +/- 1.2 nm, p less than 0.001). Neither diltiazem nor nisoldipine nisoldipine altered the basal 42K efflux or contractile activity of aorta from control-salt rats. These results suggest that the basal tension and elevated 42K efflux in aorta from aldosterone-salt hypertensive rats are supported by the entry of extracellular calcium into the tissue through potential-operated calcium channels.
authors.affiliation: Department of Physiology, University of Missouri, Columbia.
authors.forename: J M
authors.initials: JM
authors.lastname: Smith
authors.forename: A W
authors.initials: AW
authors.lastname: Jones
mesh_terms: D000450:Aldosterone; D000818:Animals; D001011:Aorta / Q000378:metabolism* / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004110:Diltiazem / Q000494:pharmacology*; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D015737:Nisoldipine / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D002121:Calcium Channel Blockers; D012965:Sodium Chloride; D000450:Aldosterone; D015737:Nisoldipine; D011189:Potassium Chloride; D004110:Diltiazem; D011188:Potassium; D002118:Calcium